Investigating the specificity of the neurologic pain signature against breathlessness and finger opposition

Figures

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  Figure 1.. Overall NPS activity in the contrasts of interest for the 2 data sets. Left: Three-dimensional representation of some of the core regions of the NPS. **Significantly different from zero at P < 0.01; #Significantly different from zero at q < 0.05 (FDR corrected). NPS, neurologic pain signature.

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  Figure 2.. (A) Regional NPS activity subregions of the NPS for the anticipation, breathlessness, and finger opposition contrasts from study 1. Significant NPS activation is observed in the dorsal anterior cingulate cortex (dACC), right thalamus (rThal), right secondary somatosensory cortex or operculum (rS2Op), and vermis for both breathlessness and finger opposition and in the right inferior parietal lobule (rIPL) for both anticipation and breathlessness. For a full list of regions please see Supplementary Table 1B, available at http://links.lww.com/PAIN/B381. (B) Univariate statistical maps (displayed using a visualisation threshold of P < 0.5) created using voxel-wise permutation testing with a cluster-forming threshold of T > 2.3 for each of the contrasts of interest. A, anticipation contrast; B, breathlessness contrast; F, finger opposition contrast. *Significantly different from zero at P < 0.05; **Significantly different from zero at P < 0.01; #Significantly different from zero at q < 0.05 (FDR corrected). NPS, neurologic pain signature.

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  Figure 3.. Regional NPS activity in the insula for the anticipation, breathlessness, and finger opposition contrasts from study 1. Robust statistical activity is observed in the bilateral insula (labelled lIns and rIns) for all 3 conditions, whereas no significant activity is observed in the right dorsal posterior insula (rdpIns). A, anticipation contrast; B, breathlessness contrast; F, finger opposition contrast. **Significantly different from zero at P < 0.01; #Significantly different from zero at q < 0.05 (FDR corrected). NPS, neurologic pain signature.

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  Figure 4.. (A) Regional NPS activity subregions of the NPS for the anticipation and breathlessness contrasts during both saline and remifentanil administration from study 2. Significant NPS activation is observed in the dorsal and pregenual anterior cingulate cortex (dACC and pgACC), right thalamus (rThal), and right secondary somatosensory cortex or operculum (rS2Op) for breathlessness, with the NPS-related activity in the right thalamus and rS2Op significantly modulated by the administration of the opioid remifentanil. For a full list of regions please see Supplementary Table 2B, available at http://links.lww.com/PAIN/B381. (B) Univariate statistical maps (displayed using a visualisation threshold of P< 0.5) created using voxel-wise permutation testing with a cluster-forming threshold of T > 2.3 for each of the contrasts of interest. A, anticipation contrast (saline); RA, remifentanil anticipation contrast; B, breathlessness contrast (saline); RB, remifentanil breathlessness contrast. *Significantly different from zero at P < 0.05; **Significantly different from zero at P < 0.01; #Significantly different from zero at q < 0.05 (FDR corrected); ✢Significantly modulated by remifentanil with…

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  Figure 5.. Regional NPS activity in the insula for the anticipation and breathlessness contrasts during both saline and remifentanil administration from study 2. Robust, positive statistically significant NPS-related activity is only observed in the bilateral insula (labelled lIns and rIns) for the breathlessness contrast, which is significantly modulated by the administration of the opioid remifentanil. Neurologic pain signature–related activity in the right dorsal posterior insula (rdpIns) is significantly decreased during saline anticipation. A, anticipation contrast (saline); RA, remifentanil anticipation contrast; B, breathlessness contrast (saline); RB, remifentanil breathlessness contrast. **Significantly different from zero at P < 0.01; #Significantly different from zero at q < 0.05 (FDR corrected); ✢✢Significantly modulated by remifentanil at P < 0.05.